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Factor VIIIa (LongAte)

✓ Approved

PolyTherics Limited · F8 · 重组蛋白

什么是 Factor VIIIa？

Factor VIIIa 是一种重组蛋白，由PolyTherics Limited研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名LongAte
公司PolyTherics Limited
药物类别重组蛋白, 细胞治疗
分子靶点F8
给药途径Injectable (Others), Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, PolyTherics Limited

作用机制

分子靶点

Factor VIIIa 作用于 1 个分子靶点：

F8coagulation factor VIII (AHF, FVIII)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

Factor VIIIa 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Congenital, familial and genetic disordersFactor VIII deficiency✓ Approved

相关研究文献

PubMedImmunity2026-06-13

Interleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity.

Yang Dandan D, Huang Linglin L, Yang Jianfei J, Etxezarreta-Arrastoa Oier O et al.

Interleukin 23 receptor (IL-23R) signaling is critical for the generation of pro-inflammatory CD4+ IL-17-producing T helper cells (Th17) that can drive autoimmune tissue inflammation, but the underlying mechanisms are not clear. We integrated phosphoproteomic and transcriptomic data downstream of IL-23R and IL-12 receptor (IL-12R), which share a common subunit, to identify mechanisms engaged specifically by IL-23. We identified chromodomain helicase DNA-binding protein 1 (CHD1), an epigenetic regulator, and the glucocorticoid receptor (GR), a transcription factor (TF), as mediators of IL-23R signaling. IL-23R activation promoted CHD1 interaction with TF STAT3 and co-binding at the TF RORγt locus to enforce a pro-inflammatory Th17 state. Conversely, IL-23R signaling altered phosphorylation of the GR, thereby preventing its activation and nuclear translocation, ultimately impairing GR-driven inhibition of pro-inflammatory Th17 gene programs. Our findings uncover two mechanisms by which IL-23 promotes a pro-inflammatory Th17 cell state, offering potential therapeutic targets for treating Th17-driven autoimmune tissue inflammation and restoring homeostasis.

PMID 42285104
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PubMedTrends in cancer2026-06-13

Aging: Barrier or catalyst of cancer?

Huna Anda A, Martin Nadine N, Bernard David D

Aging is a major risk factor for cancer, yet its role in cancer biology remains largely unexplored and often overlooked. Interestingly, studies assessing the impact of aging on oncogenic KrasG12D-driven lung tumor initiation, early progression, and metastasis have reported both pro- or antitumoral effects, which are presented and discussed herein.

PMID 42285886
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PubMedCell death & disease2026-06-13

Inflammation reprograms fibro-adipogenic progenitors to sustain immunopathogenic niches in myositis.

Nelke Christopher C, Sanchez-Dal Cin Julian J, Dallevet Charles-Antoine CA, Park Jin-Soo JS et al.

Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders defined by persistent muscle inflammation, fibrosis, and frequent resistance to current therapies. However, the mechanisms perpetuating disease activity despite immunosuppressive treatment remain elusive. Here, we describe a novel role for tissue-resident stromal cells, specifically fibro-adipogenic progenitors (FAPs), in sustaining skeletal muscle inflammation. Utilizing single-nucleus and spatial transcriptomics in 24 IIM patients and six non-diseased controls, we describe how FAPs adapt to their tissue context, favoring T-cell-centric programs in T-cell environments and myeloid programs in macrophage environments. At the spatial level, FAPs form inflammatory niches by co-localizing with muscle stem cells and activated macrophages, positioning them to participate in cell-to-cell communication with both immune and muscle cells. Trajectory and ligand-receptor analyses suggest a dual-input mechanism whereby infiltrating immune cells (via TGF-β) and myofibers (via epidermal growth factor (EGF)) converge on the AP-1 transcription factor to drive FAP differentiation toward a pro-inflammatory and pro-fibrotic phenotype. Mechanistically, exposure of primary human FAPs to TGF-β and EGF induces a primed state by altering the accessibility to AP-1 regulatory elements. Together, our findings reveal a previously unrecognized role of tissue-resident stromal cells in IIM, highlighting microenvironmental cross-talk centered on FAPs as a promising and actionable therapeutic target.

PMID 42285969
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PubMedScientific reports2026-06-13

Collagen-derived biomarkers reveal distinct fibrotic responses among cancer-associated fibroblasts.

Hettich Annika A, Karsdal Morten A MA, Willumsen Nicholas N

Cancer-associated fibroblasts (CAFs) are key drivers of extracellular matrix (ECM) deposition and remodeling in the tumor microenvironment (TME), processes that facilitate tumor progression and metastasis. However, CAFs exhibit significant heterogeneity and functional complexity, posing challenges for effective therapeutic targeting. In this study, we evaluated the production of three important ECM proteins - type I (PRO-C1), type III (PRO-C3), and type VI (PRO-C6) collagen - by CAFs in vitro. Four distinct CAFs were cultured in Ficoll-containing media supplemented with ascorbic acid for up to 12 days. Cells were stimulated with profibrotic or inflammatory factors (TGF-β1, PDGF-AB, IL-1α, IL-6) and/or treated with antifibrotic compounds (ALK5i, Fresolimumab). Collagen production was quantified in collected cell culture media using competitive ELISA. Our results reveal distinct fibrotic responses among CAFs. Two CAFs displayed high intrinsic fibrotic activity and minimal additional fibrotic responsiveness to profibrotic stimuli, whereas two CAFs exhibited low intrinsic fibrotic activity and significant increases in PRO-C1, PRO-C3, and PRO-C6 upon profibrotic stimulation. Notably, TGF-β1 was the primary driver of PRO-C3, PDGF-AB was the primary driver of PRO-C6, while IL-1α and IL-6 had no effect on PRO-C1, PRO-C3 and PRO-C6 levels. Antifibrotic treatments with ALK5i and Fresolimumab effectively reduced collagen biomarkers elevated by TGF-β1 to baseline levels or below.These results underscore the heterogeneity of CAFs in ECM remodeling, highlighting the need for tailored therapeutic strategies to target tumors exhibiting high fibrotic activity.

PMID 42286082
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PubMedJournal of the science of food and agriculture2026-06-13

Drought priming and plant growth-promoting rhizobacteria enhance Solanum lycopersicum metabolites under drought stress.

David Oyinade A OA, Fabiyi Oluwatoyin A OA, Olawuni Idowu I, Chukwuma Deborah M DM et al.

Drought stress is an important factor that consistently decreases plant productivity. Bio-stimulants such as plant growth-promoting rhizobacteria (PGPR) and arbuscular mycorrhizal fungi (AMF) have been shown to modulate stress-related pathways. The aim of this study was to enhance the metabolic memory of tomato under different drought stress conditions using these bio-stimulants. Two weeks after planting, air-dried sieved soil mixed with 150 g of Glomus deserticola and 1 mL of 1010 CFU mL-1 Enterobacter ludwigii was applied to the root zone. Drought treatments included control, drought stress, and drought priming. Drought priming increased the accumulation of proline, phenolics, and anthocyanins compared with drought stress (DS). Compared with control plants under drought priming, combining PGPR with drought priming enhanced ATPase by 81%, proline by 137%, soluble sugar by 296%, and phenylalanine ammonia-lyase by 12%. Phenylalanine ammonia-lyase is actively involved in the biosynthesis of secondary metabolites like flavonoids, which increased by 60%, and anthocyanins, which increased by 75%. An increase in biomass, a 100% survival rate, and low malondialdehyde content were observed. Combining AMF and drought priming significantly increased proline (108%), soluble sugar (240%), flavonoids, antioxidant enzymes, and phenylalanine ammonia-lyase, resulting in a survival rate of 66.67%. Plant growth-promoting rhizobacteria and AMF also enhanced the accumulation of NO, which is necessary for antioxidant enzyme accumulation. Integrating PGPR with drought priming constitutes an effective strategy for enhancing immediate stress resilience and strengthening metabolic responses. Further research using epigenetic approaches is recommended to uncover drought stress memory under drought priming, with a focus on PGPR. © 2026 Society of Chemical Industry.

PMID 42285747
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PubMedCarbohydrate polymers2026-06-13

Hierarchical construction of a superhydrophobic and superior intrinsically flame-retardant phosphorylated microcrystalline cellulose bio-based composite aerogel.

Lang Wenchao W, Jia Haoyi H, Wang Zhe Z, Wu Ningjing N

The practical deployment of cellulose aerogels in the thermal-insulation fields is severely constrained by their inherent hygroscopicity, flammability, and fragility. Integrating superior flame-retardancy with superhydrophobicity in cellulose-based aerogel remains a significant challenge. Herein, phosphorous-containing microcrystalline cellulose (PMCC) was utilized as an intrinsically flame-retardant bio-based matrix, and a hierarchical organic-inorganic network was engineered via methyltrimethylsilane crosslinking coupled with in situ self-assembly of modified silica (MSiO2) nanoparticles. The resulting MPMCC-MSiO2 composite aerogels featured a hierarchically multiscale porous architecture in which MSiO2 and poly(methylsilsesquioxane) (PMSQ) micro/nanoscale particles were uniformly integrated throughout the coarse three-dimensional pore matrix framework. This configuration of the MPMCC-MSiO2 aerogel enabled superhydrophobicity across different cross-sections with excellent self-cleaning, achieving water contact angles (WCA) up to 151°. Moreover, the organic-inorganic dual crosslinked network significantly reinforced mechanical performance, delivering compressive moduli of MPMCC-MSiO2-2 reaching 5.50 MPa, corresponding to enhancements of 491.4% relative to PMCC aerogel. Notably, the limiting oxygen index (LOI) of the MPMCC2-MSiO2-2 aerogel increased from 36.8% for the PMCC aerogel to 60.0%, attributed to the phosphorus/silicon synergistic flame-retardant effect. The integration of ultra-high flame-retardancy, superhydrophobicity, and structural robustness renders this MPMCC-MSiO2 bio-based composite aerogel promising for advanced, sustainable thermal insulation applications.

PMID 42285677
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